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- W126034612 endingPage "192" @default.
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- W126034612 abstract "Extreme complexity and a potential for cross-talk within the TLR signaling pathways suggest that mutations in almost any receptors or intracellular signaling components would result in severe innate immune deficiency. However, to date, relatively few mutations have been described that underlie deficient TLR4 signaling and increased susceptibility to infectious disease. These include mutations in TLR4, the IRAK-4 enzyme, and in NEMO (IKKγ) and IκBα components of the IKK signaling complex. Due to the central role for IRAK-4 in mediating TLR-mediated signal transduction, IRAK-4 mutations severely affect antibacterial immune defense mechanisms. This defect is associated with mutations within the kinase domain of IRAK-4 that seem to inhibit the formation of functional signaling complexes with receptor and intracellular components of the IL-1R/TLR4 pathway. This property of truncated IRAK-4 molecules also raises the possibility for therapeutic intervention in hyperinflammatory states by using IRAK-4 mimetics to inhibit signaling. Future studies will likely reveal the feasibility of such an approach, and delineate how IRAK-4 deficiency affects other antibacterial immune defense mechanisms, including development of adaptive immunity." @default.
- W126034612 created "2016-06-24" @default.
- W126034612 creator A5015698726 @default.
- W126034612 creator A5018910683 @default.
- W126034612 creator A5041046556 @default.
- W126034612 creator A5091757859 @default.
- W126034612 date "2006-01-01" @default.
- W126034612 modified "2023-10-05" @default.
- W126034612 title "IRAK-4: A key kinase involved in toll-like receptor signaling and resistance to bacterial infection" @default.
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